Traumatic Brain Injury

Alteration in brain function, or other evidence of brain pathology, caused by an external force

Alteration in brain function, or other evidence of brain pathology, caused by an external force

• leading cause of injury-related death and disability in the US

  • 1.7 million people visit emergency departments for TBI annualy

  • 50,000 people die as a result of the injury

  • 300,000 require hospitalization

• True incidence likely underestimated

  • does not include military, non-ED visits, or many sports-related injury

Prevalence of TBI

• Falls – 32%

• Motor vehicle/traffic accidents – 19%

• Struck by/against events – 18%

• Assaults – 10%

Leading Causes of TBI

• Children (0–4 years) - Most common population affected.

• Adolescents & young adults (<25 years)

• Older adults (65+ years)

• Hospitalization and death as a result of TBI is most common.

High-risk groups:

• 5.3 million people in the U.S. live with TBI-related disability.

• 1 year after injury:

  • 40% not working

  • 33% struggle with social integration

• 25% need help with ADLs

• ~40% report poor physical & mental health

Long Term Impact of TBI

• Traumatic brain injury is a heterogenous injury, with a wide variety of pathophysiological mechanisms.

• The brain damage results from external forces that cause brain tissue to make direct contact with an object (bony skull or penetrating object), rapid acceleration or deceleration forces, or blast waves from an explosion.

Mechanism of Injury and Pathophysiology

• Primary Injury

  • Due to direct trauma to the parenchyma

  • Secondary Injury

• Results from a cascade of biochemical, cellular, and molecular events that evolve over time due to the initial injury and injury-related hypoxia, edema, and elevated intracranial pressure (ICP).

Brain tissue damage can be categorized as follows:

Caused by direct trauma to brain tissue.

TBI: Primary Injury

• Contact injuries (e.g., contusions, lacerations, hematomas)

• Acceleration/deceleration injuries (e.g., diffuse axonal injury - DAI)

Main types of Primary Injury

• Anterior temporal poles

• Frontal poles

• Lateral and inferior temporal cortices

• Orbital frontal cortices.

Primary Injury: Common areas of focal injury

Diffuse axonal injury (DAI)

Predominant mechanism of injury in most individuals with severe to moderate TBI.

• Parasagittal white matter of the cerebral cortex

• Corpus callosum

• Pontine-mesencephalic junction adjacent to the superior cerebellar peduncles.

Diffuse axonal injury (DAI): Often occurs in discrete areas:

False: Mechanism is microscopic, so often there are minimal initial findings on CT & MRI.

True/False: Diffuse axonal injuries are often obvious in initial findings on CT & MRI

• Common in high-speed motor vehicle accidents (MVAs) and can be seen in some sports-related TBIs.

• Common in high-speed motor vehicle accidents (MVAs) and can be seen in some sports- related TBIs.

Diffuse axonal injury (DAI) pathophysiology & MOI

Blast Injury

Signature injury of the U.S. military conflicts in the Middle East.

Brain Injury

When an explosive device detonates a transient shock wave is produced, which can cause brain damage.

1. Primary Blast Injury

   • Direct effect of blast overpressure on organs (in this case the brain).

2. Secondary Blast Injury

   • Shrapnel and other objects being hurled at the individual.

3. Tertiary Blast Injury

   • Occurs when the victim is flung backward and strikes an object.

Types of Blast Injuries:

1. Direct transcranial blast wave propagation.

2. Transfer of kinetic energy from the blast wave through the vasculature, which triggers pressure oscillations in the blood vessels leading to the brain.

3. Elevations in cerebrospinal fluid (CSF) or venous pressure caused by compression of the thorax and abdomen and by propagation of a shock wave through the blood vessels or CSF.

Three mechanisms by which primary blast brain injury may occur:

Occurs hours to days after initial trauma.

Secondary Injury

Hypoxia, hypotension, ischemia, edema,

↑ ICP

Secondary Injury: Triggered by?

• Glutamate toxicity

• Calcium influx

• Free radical release

• Inflammatory cytokines

Secondary Injury: Cellular-level changes include:

Brain swelling, hematoma, CSF imbalance

Elevated Intracranial Pressure (ICP) is caused by?

ICP: 5–20 cm H2O

Normal ICP

• Brain herniation (uncal, central, tonsillar)

• Requires emergency treatment

High ICP can lead to:

• Cushing Triad

• Altered level of consciousness

• Headache

• Vomiting

• Papilledema

• Behavioral Changes

Elevated Intracranial Pressure Clinical Features

• Irregular breathing

• Widened pulse pressure

• Bradycardia

Cushing Triad

• macrocephaly

• bulging fontanels

• sunset sign

Elevated intracranial Pressure Clinical features in infants

• Impaired motor function:

  • Upper extremity (UE) and lower extremity (LE) paresis.

  • Impaired coordination

  • Impaired postural control

  • Abnormal tone

  • Abnormal gait

*may be present as life-long impairments.

2. Abnormal, involuntary movements (tremors, chorea and dystonic movements) are less common.

3. Patients may also present with impaired somatosensory function, depending on the location of the lesion.

Sequelae of Traumatic Brain Injury: Neuromuscular

• Involves arousal, attention, concentration, memory, learning, and executive functions (Categories: planning, cognitive flexibility, initiation and self-generation, response inhibition, and serial ordering and sequencing).

• Mainly controlled by the frontal lobes, making them vulnerable in TBI.

• Altered levels of consciousness are commonly seen.

• Disordered arousal states seen after severe brain injury:

  • Coma

  • Vegetative State

  • Minimally Conscious State

Sequelae of Traumatic Brain Injury: Cognitive

Cognition

The mental process of knowing and applying information.

• The arousal system is not functioning.

• The patient’s eyes are closed.

• No sleep/wake cycles.

• Patient is ventilator dependent.

• No auditory or visual function.

• No cognitive or communicative function.

• Abnormal motor and postural reflexes may be present.

• Usually not permanent.

• Patients may become brain dead, enter a vegetative or minimally conscious state, or go onto full recovery.

Cognitive Impairments: Coma

• Disassociation between wakefulness and awareness.

• Higher CNS centers are not integrated with the brainstem.

  • patient can be weaned off the ventilator.

• Present sleep/wake cycles.

• Eyes may be open though awareness of surroundings is absent.

• Patients may startle to visual or auditory stimuli and briefly orient to sound or visual stimuli.

• Meaningful cognitive and communication function is absent.

• Reflexive smiling/crying may be present.

• A withdraw response to noxious stimuli is present.

• Although patients in a vegetative state may appear to have purposeful movement, these movements are non purposeful and reflexive in response to external stimuli.

• Patients in a permanent vegetative state may have no meaningful motor or cognitive function and a complete absence of awareness of self or the environment for period greater than 1 year after TBI and greater than 3 months after anoxic brain injury.

Cognitive Impairments: Vegetative State

• There is minimal evidence of self or environmental awareness.

• Cognitively mediated behaviors occur inconsistently and are reproducible or sustained such that they can be differentiated from reflexive behaviors.

• Present sleep/wake cycles.

• Patients can localize to noxious stimuli, inconsistently reach for objects, may localize to sound location and demonstrate sustained visual fixation and visual pursuit.

Cognitive Impairments: Minimally Conscious State

an unresponsive state from which the patient can be aroused only briefly with vigorous, repeated sensory stimulation.

Cognitive Impairments: Stupor

the patient sleeps often and when aroused exhibits decreased alertness and interest in the environment and delayed reactions.

Cognitive Impairments: Obtunded

• Patients can exhibit profound behavioral changes as they progress through recovery.

• These impairments can be closely linked to cognitive impairments and are often more debilitating in the long run than physical disability.

• Common behavioral sequelae:

  • Low frustration tolerance

  • Agitation

  • Disinhibition

  • Apathy

  • Emotional lability

  • Mental inflexibility

  • Aggression

  • Impulsivity

  • Irritability

Sequelae of Traumatic Brain Injury: Neurobehavioral

• Language and communication deficits after brain injury are generally non-aphasic in nature and are related to cognitive impairment.

• Common language and communication deficits include disorganized and tangential oral or written communication, imprecise language, word retrieval difficulties, and disinhibited and socially inappropriate language.

• Patients may also exhibit difficulties communicating in distracting environments, reading social cues, and adjusting communication to meet the demands of the situation.

• These communication deficits can affect employability, social integration, and quality of life.

Sequelae of Traumatic Brain Injury: Communciation

Paroxysmal Sympathetic Hyperactivity (PSH)

• These episodes are paroxysmal, meaning they occur suddenly and unpredictably, and are usually triggered by external stimuli (like pain, suctioning, or repositioning).

is a clinical syndrome often seen after severe traumatic brain injury (TBI). It is characterized by sudden, episodic increases in sympathetic nervous system activity.

• Tachycardia

• Hypertension

• Hyperthermia

• Tachypnea

• Sweating

• Posturing

Key Features of Paroxysmal Sympathetic Hyperactivity (PSH)

• Typically results from disruption of brain pathways that regulate the autonomic nervous system, especially following diffuse axonal injury or severe cortical/subcortical trauma.

• It involves an imbalance between excitatory and inhibitory control of the sympathetic system.

Paroxysmal Sympathetic Hyperactivity (PSH): Causes and Pathophysiology:

• Reducing external stimuli

• Medications: beta-blockers, opioids, benzodiazepines, and others to control symptoms

• Supportive care and close monitoring.

Paroxysmal Sympathetic Hyperactivity (PSH): Management

• Seen in 12% and 50% of people with severe TBI.

• Phenytoin (an anticonvulsant) is effective in decreasing the risk of early post-traumatic seizures.

Post-traumatic Seizures

• DVT

• Heterotropic ossification

• Pressure olcer

• Pneumonia

• Chronic pain

• Contractures

• Decreased endurance

• Muscle atrophy

• Fracture

• Peripheral nerve damage

Secondary Impairments and Medical Complications

Glasgow Coma Scale

The most widely used clinical scale that measures level of consciousness and helps define and classify the severity of injury.

• Motor Response (6pts)

• Verbal Response (5pts)

• Eye Opening (4pts)

GCS is comprised of three response scores

• Mild: 13 to 15

• Moderate: 9 to 12

• Severe: ≤ 8

The scores from the separate responses are summed to provide a score between 3 and 15.

GCS Scoring

Mild TBI
LOC	0-30 mins
AOC	brief >24 hours
PTA	0-1 day
GCS	13-15
Neuroimaging	normal

Characteristics of Mild TBI: LOC, AOC, PTA, GCS, Neuroimaging

Moderate TBI
LOC	>30 min and <24 hr
AOC	>24 hours
PTA	>1 and <7 days
GCS	9-12
Neuroimaging	normal or abnormal

Characteristics of Moderate TBI: LOC, AOC, PTA, GCS, Neuroimaging

Severe TBI
LOC	>24 hours
AOC	>24 hours
PTA	>7 days
GCS	<9
Neuroimaging	normal or abnormal

Characteristics of Severe TBI: LOC, AOC, PTA, GCS, Neuroimaging

Factors that can be useful in estimating future outcomes:

• Low initial scores on the GCS, particularly motor score and pupillary reactivity, have been identified as a predictor of poor recovery in patients with moderate to severe TBI.

• Other factors associated with poor outcomes are age, race, and lower education level.

• Petechial hemorrhages, subarachnoid bleed, obliteration of 3rd ventricle or basal cisterns, midline shift, and subdural hematoma findings on initial CT scan are also predictive of poor outcomes.

The Medical Research Council (MRC) CRASH (corticosteroid randomization after significant head injury) study

provides a Web-based calculator that allows clinicians to enter demographic and prognostic information and calculate the 14-day mortality risk and unfavorable outcome at 6 months, along with the 95% confidence interval.

Post-Traumatic Amnesia

Time between injury and consistent memory of ongoing events

Likely to be living without assistance.

PTA outcomes: <53 days

Higher Functional Independence Measure (FIM) scores at discharge from inpatient rehabilitation.

PTA outcomes: <48.5 days

Likely to have a good overall recovery (as measured by the GOS).

PTA outcomes:<34 days

Likely to be employed.

PTA outcomes:<27 days

• Ensure patient is medically stable before contact.

• Identify:

  • ICP monitoring

  • Ventilator status

  • ROM & weight-bearing precautions

  • Musculoskeletal injuries or open wounds

• Understand contraindications and precautions.

Patient Examination: Step 1 medical Record

Patients in coma, vegetative, or minimally conscious states may exhibit:

• Abnormal tone (e.g., spastic hypertonia)

• Primitive postures:

  • Decorticate rigidity

  • Decerebrate rigidity

Patient Examination: Severe TBI

UE flexion, LE extension

Decorticate rigidity

UE and LE Extension

Decerebrate rigidity

No Response

• patient appears to be in deep sleep and is completely unresponsive to any stimuli

Rancho Los Amigos Levels of cognitive Functioning: I

Generalized Response

• patient reacts to inconsistently and nonpurposefuly to stimuli in a nonspecific manner

• responses are limited and often the same regardless of stimulus presented

• responses may be physiological changes, gross body movements, and/or vocalization

Rancho Los Amigos Levels of cognitive Functioning: II

Localized Response

• patient reacts specifically but inconsistently to stimuli

• responses are directly related to the type of stimulus presented

• may follow simple commands such as closing eyes or squeezing hand in an inconsistent, delayed manner

Rancho Los Amigos Levels of cognitive Functioning: III

Confused-Agitated

• patient is in a heightened state of activity

• behavior is bizzarre and nonpurposeful relative to immediate environment

• Does not discriminate among persons or objects; is unable to cooperate directly with treatment efforts

• Verbalizations frequently are incoherent and/or inappropriate to the environment; confabulation may be present

• Gross attention to environment is very brief; selective attention is often nonexistent

• patient lacks short and long-term recall

Rancho Los Amigos Levels of cognitive Functioning: IV

Confused-Inappropriate

• patient is able to respond to simple commands fairly consistently

• However, with increased complexity of commands or lack of any external structure, responses are nonpurposeful, random, or fragmented

• Demonstrates gross attention to the environment but is highly distractible and lacks ability to focus attention on a specific task

• With structure, may be able to converse on a social automatic level for short periods of time

• Verbalization is often inappropriate and confabulatory

• Memory is severely impaired; of often shows inappropriate use of objects; may perform previously learned tasks with structure but is unable to learn new information

Rancho Los Amigos Levels of cognitive Functioning: V

Confused-Appropriate

• patient shows goal-directed behavior but is dependent on external input or direction

• follows simple directions consistently and shows carryover for relearned tasks such as self-care

• Responses may be incorrect due to memory problems, but they are appropriate to the situation

• Past memories show more depth and detail than recent memory

Rancho Los Amigos Levels of cognitive Functioning: VI

Automatic Appropriate

• patient appears appropriate and oriented within the hospital and home settings

• goes through routine automatically, but frequently robot-like

• Patient shows minimal to no confusion and has shallow recall of activities

• Shows carryover for new learning but at a decreased rate

• With structure is able to initiate social or recreational activities; judgement remains impaired

Rancho Los Amigos Levels of cognitive Functioning: VII

Purposeful-Appropriate

• patient is able to recall and integrate past and recent events and is aware of and responsive to environment

• Shows carryover for new learning and needs no supervision once activities are learned

• May continue to show a decreased ability relative to premorbid abilities, abstract reasoning, tolerance for stress, and judgement in emergencies or unusual circumstances

Rancho Los Amigos Levels of cognitive Functioning: VIII

Basilar skull fracture following head trauma

Battle sign and racoon eyes are both late signs of?