TBI Midterm

TBI

head injury, head trauma, traumatic closed head injury, closed head trauma, non-focal brain damage

• 40% of deaths from acute injuries

• Most common in males ages 15-24, elderly>75

• Most common causes: MVAs(motor vehicle accidents), falls, and assaults

Patterns of Injury

• focal

• diffuse

Mechanism of Injury

• contact forces

• inertial forces (translational and rotational acceleration)

contact forces-types of injury

• skull fracture

• epidural hematoma

• coup contusion

• subdural hematoma

Inerial Forces(translational acceleration)-Types of Injury

• contracoup contusion

• intracerebral hematoma

• subdural hematoma

Inertial Forces(Rotational Acceleration)-Types of Injury

• concussion

• diffuse axonal injury

• subarachnoid hemorrhage

• intraventricular hemorrhage

• tissue tear hemorrhage

• gliding contusion

concepts of consciousness

1. Active process

2. Wakefulness or alertness

3. Self-awareness of one’s own cognition and mental processes

4. Focus of attention or filtering

5. Motivation is an internal drive

6. Working memory is used for decisions and actions

7. The brain can relate remembered events to each other

8. Decision-making capacity for action is dependent on attention

9. Cognition involves components of consciousness

Neural Correlates of Components of Consciousness

1. Alertness

2. Attention

3. Sensation and perception

4. Perceptual-motor integration

5. Motivational system

6. Memory

7. Cognition

types of severe brain injuries

1. coma

2. vegetative state

3. minimally conscious state

4. emerging from a minimally conscious state

coma

a state of unconsciousness in which the eyes are closed, cannot be aroused, absence of sleep-wake cycle, no purposeful motor activity, no response to commands.

• Lesion affecting both hemispheres or white matter, bilateral thalami, or paramedian tegmentum

Vegetative State

inability to interact with others, no awareness of self or environment, may have spontaneous arousal, follows after a coma, caused by a diffuse arousal injury after TBI, no sustained, purposeful responses to auditory, visual, or tactile stimuli; no evidence of language comprehension or expression

• Persistent VS: Diagnosed after 1 month post-TBI

• Permanent VS: Diagnosed after 12 months post-TBI

Minimally Conscious State

Severely altered consciousness with minimal but definite behavioral evidence of awareness

• Represents improvement from coma or vegetative state

• Associated with Grade II/III diffuse axonal injury (DAI), multifocal cortical lesions, and occasionally thalamic lesions

• Preserved cortico-thalamic connections support limited cognitive processing

Identifying Behaviors:

• Follows simple commands

• Intelligible verbalizations

• Consistent yes/no responses

• Emotion or movement responses to environmental stimuli

Emerging from a minimally conscious state

Behaviors characteristic of EMCS:

• Active communication (verbal, gestural or through AAC devices)

• Functional object use which requires discrimination of items presented

• Symptoms to be reliable & consistent

Severe TBI: Prognosis

1. Prognostic significance of injury severity

2. Classification schemes

3. Diffuse axonal injury

4. Contusion

5. Anoxia

6. Prognostic significance of age

7. Associated injuries

8. Premorbid status

9. Other indicators: post-traumatic electrophysiologic abnormalities

Emergency Medical Services

• Trauma systems since the 1980s have cut TBI mortality from 50% to 25%.

• Patients are routed to Level I/II trauma centers for specialized emergency care.

Acute Hospital Care

• Severe TBI patients need ICU monitoring and early rehab planning.

• Rehab type (inpatient, subacute, or SNF) depends on medical stability and recovery speed.

Acute Inpatient Rehabilitation (AIR)

Provides intensive rehab (≥3 hours/day) and 24-hour medical care for patients with significant functional deficits who are medically stable.

Subacute/SNF Rehab

Lower-intensity rehab for patients with slow recovery or persistent impairments. Includes neurobehavioral units; care may last months.

Outpatient Rehab

Offers therapy services (PT, OT, SP) with flexible intensity based on needs and insurance. Rehab is less coordinated and can occur in home or community settings.

Residential Rehab

Group living with therapy and support for independent living. Serves patients not ready for home, with gradual progression to community reintegration.

Vocational Services

Focuses on return to work through training, education, and on-site support. Most effective when linked with outpatient rehab.

Special Education

Provides school-based support for children with TBI under IDEA (1990), using IEPs to meet educational needs after rehab.

Community-Based Services

Includes support groups and home/community services to promote social and functional living skills. Often coordinated through BIAA chapters.

Causes of TBI

• Falls(#1 cause espeically in older adults or little children)

• Assaults

• Motor Vehicle Accidents

• Sports/Recreation Injuries

• Abusive Head Trauma (Shaken Baby Syndrome)

• Gunshot Wounds

• Workplace Injuries

• Child Abuse

• Domestic Violence

• Military Actions (Blast Injury)

Mechanical Causes

1. impact load

2. impulsive load

3. static or quasistatic loading

impact load

collision of the head with a solid object at an appreciable velocity (hitting the head against a car seat)

• The brain doesn’t just go back and forth, it twists, causing damage to the axon (breaks off and releases chemicals to cause more damage)

Impulsive load

sudden motion of the head without significant physical contact (whiplash)

• Mostly conscious

• White matter damage

Static or quasistatic loading

the consequences of the speed of occurrence are not significant (the brain being squeezed)

• Rare and can be fatal

Types of head acceleration

1. translational acceleration

2. rotational acceleration

3. angular acceleration

translational acceleration

uncommon, center gravity of the brain moves in a straight line, focal injuries (contrecoup, intracerebral, and subdural hematomas)

Rotational acceleration

brain rotation without the center of gravity of the brain moving, high injuries, high surface strain, deep surface strain

angular acceleration

most common, compound of translational and rotational; head’s center of gravity moves around the center of angulation; rotation produces strain on the surface and deep within the brain, injuring the white matter

Diffuse Axonal Injury

• Results from strong rotational forces or shaking (e.g., car accidents, shaken baby syndrome).

• Causes widespread tearing of nerve tissue due to angular acceleration; often occurs without direct impact.

DAI-Strich Hemorrhage

Small tissue tears in deep brain areas, disrupting axons and small vessels are indicators

Common Locations: DAI-strich hemorrhage

• Corpus callosum

• Third ventricle walls (hypothalamus, fornix, anterior commissure)

• Internal capsule

• Basal ganglia

• Dorsolateral brainstem

• Superior cerebellar peduncles

• Gray-white matter interface (especially vulnerable to shear injury)

Contusion

bruise on the brain caused by a force(blow or jolt) to the head; bruising causes bleeding and swelling inside brain; may occur with skull fractures or subdural or epidural hematomas

Gliding Contusion

Strich lesions occur in the superomedial frontoparietal white matter when angular acceleration causes the brain to move within the skull, placing tensile strain on cortical veins—if these rupture, a subdural hematoma results; if deeper vessels fail, a gliding contusion occurs.

Skull Fractures

1. depressed

2. diastatic

3. linear

4. basilar

depressed skull fracture

an object strikes the head(hit by a hammer)

Diastatic Skull Fracture

occurs in suture lines in skull

Linear Fracture

most common, ,break in skull in a straight line without displacement or depression of bone

Basilar Fracture

associated with injuries to cranial nerves; caused by either direct impact to the occiput, mastoid prominence, or supraorbital area (back of the head)

Intracranial Hematoma

• Blood clots in or around the brain

• Classified by their location in the brain

• Mild to severe to life-threatening

Types of Intracranial Hematoma

1. subdural

2. epidural

3. subarachnoid

4. intraventricular

Subdural

blood clot underneath the skull and dura but outside of the brain

Epidural

caused by local impact loading to the skull of the underlying dural veins or arteries; blood clots under the skull, but on top of the dura (the tough covering that surrounds the brain caused by a tear in an artery that runs just under the skull)

Subarachnoid

from angular acceleration that produces strain sufficient to damage to the superficial vessels running in the subarachnoid space

Intraventricular

from a very severe force; due to an impact along the sagittal diameter of the skull; negative pressure

Types of Herniation

1. subfalcine

2. central transtentorial

3. uncal

subfalcine herniation

cingulate gyrus is shifted beneath the falx cerebri when an expanding mass lesion causes medial shift of the ipsilateral hemisphere

central transtentorial herniation

caused by mass lesion in the frontal, parietal, or occipital lobes

uncal herniation

compression of the ipsilateral cerebral peduncle and posterior cerebral artery

coup-contrecoup injury

• Contusions that are both at the site of the impact and on the opposite side of the brain.

• This occurs when the force impacting the head is not only great enough to cause a contusion at the site of impact but is also able to move the brain and cause it to slam into the opposite side of the skull.

coup

bruising related to site of impact; result of excessive strain; creates negative pressure

contrecoup

causes abrasion on other side of skull

penetrating injury

occurs from the impact of a bullet, knife, or other sharp object that forces hair, skin, bone, and fragments from the object into the brain

Abusive Head Trauma (Shaken Baby Syndrome)

• occurs when the brain gets aggressively shaken; forceful whiplash motion causes the brain to be injured

• Blood vessels between the brain and skull rupture and bleed

• The accumulation of blood causes the brain tissue to compress while the injury causes the brain to swell

Closed Head

• Injury to the brain caused by an outside force without any penetration of the skull

• When the brain swells, it has no place to expand; this causes an increase in intracranial pressure, which is the pressure within the skull

Open Head

also known as a penetrating head injury, is a head injury in which the dura mater (the outer layer of the meninges) is breached.

Immediately Following a Brain Injury

• Brain tissue reacts to the trauma from the injury with a series of biochemical and other physiological responses.

• Substances that once were housed safely within these cells now flood the brain, further damaging and destroying brain cells in what is called secondary cell death.

• Depending on the severity of brain injury, effects may include temporary loss of consciousness or coma, respiratory (breathing) problems, and/or damaged motor functions.

Mild TBI

• Brief, if any loss of consciousness

• Vomiting and dizziness

• Lethargy

• Memory loss

Moderate Brain Injury

• Unconsciousness up to 24 hours

• Signs of brain trauma

• Contusions or bleeding

• Signs of injury or neuroimaging

• Memory impairment is the most persistent and disabling symptom.

• Emotional changes include blunted affect (prefrontal injury), emotional lability, impulsivity, disinhibition, and difficulty recognizing others’ emotions (especially with right hemisphere damage).

• Behavioral regulation is impaired, leading to socially inappropriate acts and denial of problems, which can hinder rehab motivation and compliance.

Severe Brain Injury

• Unconsciousness exceeding 24 hours (coma)

• No sleep/wake cycle during loss of consciousness (LOC)

• Signs of injury appear on neuroimaging tests

Locked in Syndrome

A rare neurological condition in which a person cannot physically move any part of their body aside from their eyes

Brain Death

A person with brain death is not alive because all of the brain functions, including the brain stem, no longer work

Concussion/Mild TBI

• Most common TBI, caused by direct impact or sudden head movement (e.g., whiplash); may result in brief loss of consciousness or just feeling dazed.

• Typically involves mild diffuse axonal injury (DAI) from inertial forces; may cause temporary or permanent neurological damage, even without visible imaging findings.

• A concussion is manifested by a loss of consciousness lasting less than an hour, but no more than 24 hours

• Confusions and amnesia are the hallmarks; symptoms of confusion include vacant stare, disorientation, delayed verbal and motor responses, and poor concentration or attention

Symptoms of mTBI

• somatic

• sensory

• cognitive

• cognitive complaints

• behavioral

• emotional

somatic

headaches, fatigue, sleep disturbances, nausea

sensory

dizziness, balance issues, blurred/double vision, tinnitus, sensitivity to light/noise

Cognitive

slowed processing speed, memory difficulties (new info, prospective memory), poor attention/concentration, word-finding issues, difficulty with problem solving and organization

Cognitive Complaints

Slower task completion, Easily distracted, Trouble multitasking, Forgetting intentions or recent events

Behavioral

Irritability, social withdrawal, apathy, mood swings

emotional

depression, anxiety, anger, frustration

Syndromes Associated with TBI

Postconcussion syndrome, Frontal lobe syndrome, Temporal lobe syndromes, Behavioral disorders, Cognitive deficits, Personality changes, Mood disorders, Sleep disorders, Posttraumatic epilepsy, Psychosis/accident neurosis, Aggression

Frontal Lobe Syndrome

• Common after TBI, causing behavioral dyscontrol (impulsivity, aggression), apathy, executive dysfunction, and mood issues.

• Dorsolateral frontal damage → dysexecutive syndrome; orbitofrontal damage → disinhibition; mesial frontal damage → apathy.

Temporal Lobe Syndrome

• Damage leads to language, memory, and behavioral disturbances.

• Dominant hemisphere injury causes aphasia and sensory integration problems; also amnestic and mood/behavior disorders.

Post Concussion Syndrome (PCS)

• Occurs after mild TBI with physical, cognitive, and emotional symptoms lasting ≥3 months.

• Symptoms include fatigue, headache, sleep disturbances, irritability, anxiety, and cognitive difficulties.

• Causes significant social/occupational impairment without other mental disorder explanations.

Persistent Post Concussive Syndrome (PPCS)

• PCS symptoms persist beyond 3–6 months with common anxiety, depression, chronic pain, and cognitive disruptions.

• Symptoms: headache, dizziness, sensitivity to light/noise, fatigue, memory and attention problems, mood disturbances.

• Pain and medication effects complicate recovery, impacting sleep, relationships, and alertness.

Secondary Impact Syndrome

• also termed “recurrent traumatic brain injury,” can occur when a person sustains a second traumatic brain injury before the symptoms of the first traumatic brain injury have healed.

• The second injury may occur from days to weeks following the first. Loss of consciousness is not required. The second impact is more likely to cause brain swelling and widespread damage.

Chronic Traumatic Encephalopathy(CTE)

Repeated brain trauma can result in early dementia or neurodegenerative brain disease

Built up of toxic protein tau

autonomic nervous system

• Disruption in the regulation of ANS control

• Affects the balance between sympathetic and parasympathetic output

• Cardiovascular rhythm, metabolism, and temperature regulation

• Difficulty shifting heart rate control from parasympathetic to sympathetic control at the onset of exercise

Timelines

• Acute injury adults: 0-14 days

• Acute injury kids/teens: 0-30 days

• Subacute injury: 1-3 months

• Persistent (chronic): 3+ months

Concussion can cause:

• Sleep disruption: decreased mental efficiency

• Fatigue-brain drain: attention, concentration, and speed of processing

• Headache: dizziness, balance problems, and nausea

• Mood changes: depression, anxiety, irritability

• Panic attacks

• Seizures: result of multiple concussions

Concussion Defects:

• Attention and processing-following directions, turn-taking, task initiation, shifting topics

• Memory and executive skills-self monitoring, scheduling, sequencing, planning/organizing

• Social communication and cognition-impaired ToM, decreased social participation

• Visual-vestibular changes: blurry, double vision

• Auditory processing

• Verbal expression

• Reading: decreased speed, comprehension, story retells

• Writing: increased syntactic errors, word-level errors, linearity, and cohesion

• Speech disorders: voice and fluency

Role of SLP in Concussion

• Evaluation of language, executive skills, attention, concentration, speed of processing, short term memory

• Treatment

• Education & awareness

Treatment of Concussion

• Medical/pharmacologic management (cognitive, somatic, behavioral symptoms) → attention and memory

• Neuropsychological/psychological

• Vestibular/balance

• Rehabilitation (cognitive, vestibular, and psychological)

• Biofeedback

• Nutrition

• Mindfulness

Type of Blast Injuries

1. primary blast injury

2. physical penetration

3. tertiary blast injury

4. quaternary blast injury

primary blast injury

• Result of rapid changes in atmospheric pressure that is created by the blast wave

• Results in displacement, stretching, and shearing forces

• Air-filled cavities such as the lungs and middle ear are most susceptible to damage

Physical Penetration

Explosive device fragments or other objects projectiles causes by the blast that enter the head

Tertiary Blast Injury

Injury as a result of being thrown, pushed, or shoved into another object

Quaternary Blast Injury

Injuries from burns or inhalation of hot explosive gases

symptoms of bTBI

Headache, tinnitus, nausea, memory deficits, attention deficits, EF disorders, PTSD, auditory and visual impairments

neuroanatomy affected by blast injuries

Middle cerebellar peduncles

Cingulate gyrus and cingulum bundles

Right orbitofrontal white matter

Hypothalamic pituitary axis

Medial temporal lobe

Upper brainstem

Temporal lobe

Prefrontal

Hippocampus

Long coursing white matter fibers (corpus callosum and fornix)

Corpus callosum

Fornix

Brainstem

bTBI Results

• Auditory deficits

• Auditory processing deficits

• Dual sensory deficits-visual perceptual deficits(nonverbal cues) and auditory deficits(interpreting tone)

• Cognitive deficits→ attention, working memory, executive functioning(planning, organization, problem solving, and mental flexibility)

• PTSD

• Language deficits: word finding and recall of names

  Higher level of language

bTBI treatment

• Functional strategies & Compensatory strategies

• Environmental

• Reducing anxiety

• Memory

• Computer programs

• Auditory processing

• Cueing devices

• Social skills

SLP role in critical care

Evaluation

Goal-directed treatment

Family and staff education (inservice)

Patient Observation

• record baseline vital signs

• bedside observation include:

  • Purposeful movements, decerebrate or decoricate posturing, agitated movements, spontaneous eye opening/movements, oral motor movements, facial symmetry, upper vs. lower extremities

Evaluation of Cognition, Alertness, and Arousal:

• Begin with name-calling, then tactile and, if needed, noxious stimulation; document type, consistency, and timing of responses.

• Monitor vitals; stop stimulation if unstable; observe posturing (decorticate vs. decerebrate) to assess CNS involvement.

• If responsive, test auditory comprehension considering language and physical limits; note delays, consistency, and perseveration.

Visual Response

• Assess spontaneous and stimulated eye opening; examine pupil symmetry, reaction, gaze (conjugate/dysconjugate), fixation, and tracking.

• Dysconjugate gaze may indicate brainstem involvement and can affect visual processing.

• Use OT evaluation for additional cranial nerve and visual system insights.

Oral and Motor Responses

• Observe spontaneous facial and oral movements for symmetry, strength, and intent to assess cranial nerve function.

• Check cough strength (reflexive/voluntary) for speech/swallow implications; note any impact from facial injuries or intubation.

• Use gustatory stimuli to assess cranial nerves VII and IX; identify abnormal oral reflexes.

SLP Treatment Objectives

• Responsiveness/interaction with the environment

• Cognition and language→attention, orientation, and auditory comprehension

• Communicative intent→multiple modaties

• Vocal fold integrity→airway protection, behavior, communication

• Tracheostomy tubes→speaking tubes/values

• Oral feeding→compensation techniques

• Co-treatments with other therapists (OT, PT)