Primer on Moderate – Severe TBI Incidence Pathophysiology Neuropsychological deficits Outcome

Traumatic Brain Injury According to the CDC, in 2013, there were 2.5 million ED visits for some type of TBI in the US. In 2013, there were approx. 50,000 deaths due to TBI.

Traumatic Brain Injury Causes: May occur in motor vehicle accidents, bicycle accidents, falls, assaults, contact sports, combat (blast injury).

Traumatic Brain Injury Mechanism of TBI (1) Direct blow or trauma to the head (the head being struck by an object; the head striking an object); (2) indirect blow: acceleration/deceleration forces transmitted to the head from physical trauma/blow; (3) external force (blast wave; atmospheric pressure waves) passing through or impacting the brain that results in various types of structural brain damage and physiological disruption of brain functioning resulting in various deficits and impairments in one’s neurological, physical, cognitive and behavioral status.

Traumatic Brain Injury Moderate TBI Glasgow Coma Scale score: 9 - 12 Post-traumatic Amnesia: > 24 hrs - < 7 days Length of LOC: 30 min – 24 hrs Brain abnormalities on imaging

Traumatic Brain Injury Severe TBI Glasgow Coma Scale score: 3 - 8 Post-traumatic amnesia: > 7 days Length of LOC: > 24 hrs Brain abnormalities on imaging

TBI Pathophysiology involves two primary forms of structural damage: diffuse axonal injury, and contusions. DAI refers to the stretching, twisting and/or tearing of axons that occurs throughout the brain that renders the axons (and by extension the neuron) either temporarily dysfunctional or permanently damaged.

TBI

TBI

TBI

TBI DAI occurs from physical forces acting on the white matter within the brain. Shearing force – unaligned forces pushing one part of the brain in one direction and another part of the brain in the opposite direction. Rotational force (most salient) – the head and brain are being rotated, which causes the axons to twist resulting in either temporary or permanent damage to the axon and neuron.

TBI Contusions (bruise): brain tissue damage due to diffusely spread microvascular bleeding. Occurs when the soft brain jars against the skull and bony ridges inside the skull.

TBI Contusions occur most often in the prefrontal region and anterior temporal region

TBI Two other major pathophysiological effects of TBI Diffuse (multifocal) vascular injury. Various physical forces (e.g., shearing and rotational forces) may cause tearing to small blood vessels, which result in multiple small hemorrhages.

TBI Widespread neurochemical and neurometabolic dysfunction. Disruption/dysregulation of the chemistry involved in cellular functioning (sodium – potassium pump). Disruption of ATP, fuel of cellular energy (adenosine triphosphate) Disruption/dysregulation of glucose metabolism.

TBI Chemical imbalances: For example, glutamate, an excitatory neurotransmitter, is released after TBI. Too much glutamate will excessively stimulate neurons leading to metabolic exhaustion or to the formation of free radicals with toxic effects on the nerve cell.

TBI In all cases of moderate and severe TBI, the primary pathophysiology include: Diffuse axonal injury Contusions Diffuse micro/small vessel injury Widespread cellular dysfunction, neurochemical dysregulation, neurometabolic disruption, neurotransmitter imbalances.

TBI There can also be secondary or delayed consequences from a TBI, such as: Hematoma Infection Anoxia/hypoxia: insufficient oxygen to the brain Seizures Raised intracranial pressure

TBI It has been estimated that in cases of severe TBI there are hundreds of millions to a couple - few billion neurons that are directly temporarily dysfunctional or permanently damaged.

TBI TBI is a diffuse, multifocal brain injury. There is widespread brain damage.

Neuropsychological Effects Post-acute consequences Wide ranging outcomes Wide ranging patterns of residual cognitive-behavioral deficits. In Moderate and severe TBI, there is some range and magnitude/degree of residual neurological, physical, functional, cognitive, and/or behavioral deficits.

Attention Shorter attention span Distractibility Impaired divided attention Impaired sustained attention More prone to errors Difficulty multitasking Attention fluctuates per cognitive load and environmental demands

Memory Episodic memory impairment Deficits in both encoding and retrieval Free recall < cued recall < recognition

Language Typically do not see classic aphasia syndromes in TBI. Less likely to see significant language deficits. Primary language zones are typically less damaged in TBI. Word finding problems. Need to re-read information Need more time to comprehend info

Language Difficulty writing lengthy or complex papers, owing to deficits in the interface of language and executive functions.

Speed of Information Processing Slower processing information Slower completing cognitive tasks

Cognitive Fatigue Lowered cognitive stamina and endurance.

Executive Cognitive Functions Deficits in Abstract Reasoning Problem solving Organization Planning Decision making

Executive Behavioral Functions Impaired self-regulation of behavior: A person’s ability to modulate, activate and/or depress cognitive, behavioral and emotional responses in order to achieve a desired outcome. Impaired self-monitoring of behavior: A process of tracking, evaluating and correcting one’s actions and behavior.

Executive Behavioral Deficits Behaviors of excess Disinhibition Impulsivity Quick to get irritable or agitated Social skills – Verbose, interruptions

Executive Behavioral Deficits Behaviors of inaction Apathy / Adynamia Drive, motivation Initiation Follow through

Awareness Unawareness may be defined as a global to discrete, severe to mild, lack of recognition, experience or perception of deficits that is neurologically mediated. Thus, there is some degree of disparity between one’s self-appraisal vs their actual level of functioning.

Emotional – Psychological Issues Depressed mood Grief Anger/frustration Uncertainty Change in self-identity Loss of purpose and meaning

Outcome

Outcome