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Clinical and Neuropsychology - 1 > NPch15 Traumatic Brain Injury > Flashcards

NPch15 Traumatic Brain Injury Flashcards

1
Q

Traumatic brain injury

A

An alteration in brain function or pathology due to external force
- Physical trauma

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2
Q

What are two types of TBI?

A
  1. Closed head injury (CHI)
  2. Penetrating head injury (PHI)
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3
Q

Acquired Brain Injury

A

Any type of damage to the brain that occurs after birth
- TBI is the most common type of ABI among people under 50 yrs
- Other aetiologies, like stroke belong under ABI

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4
Q

Epidemiology of TBI - how common is it?

A
  • Most common cause of brain damage in children and young adults
  • Recent data suggest approximately 85,000 people per year in the Netherlands (underestimate - many not hospitalised)
  • Increasing rate of TBI in older people due to ageing population and higher survival rates
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5
Q

Incidence

A
  • Peak ages: 15-24 yrs, first 5 yrs and elderly
  • Men sustain TBIs twice as frequently as women (men engage in behaviours that result in TBI more often)
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6
Q

What are risk factors contributing to TBI?

A
  • Lower SES, uneployment, and lower education (probably because of the behaviours these people engage in)
  • Alcohol and substance abuse significantly contribute to TBI incidence (no enough reflexes to stop the fall, agression)
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7
Q

What are main causes of TBI?

A

Falls, transportation-related injuries (cars, motorbikes) and blows to the head caused by violence

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8
Q

What are long-term implications of TBI?

A
  • Long-term mortality associated with age, lack of independence, and tube feeding
  • Late-life dementing illnesses and neuropsychochiatric sequlae common
  • Specific risks in retired athletes, e.g. rugby or American football
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9
Q

How can we distinguish between the different phases TBI is in, in regard to recovery?

A
  1. Acute phase (which lasts up to 1 month)
  2. The subacute phase (lasting up to 6 months)
  3. The chronic phase
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10
Q

Classification

How do we classify TBI based on severity? What are the different effects?

A
  • TBI severity spectrum
  • Mild impacts leave no lasting effects
  • Severe TBIs can lead to prolonged coma and extensive brain damage
  • Severity correlated with long-term social and cognitive effects
  • Glasgow coma scale (GCS)
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11
Q

What is Glasgow Coma Scale? What are the 3 domains? How do you interpret the score?

A
  • Used to test the spontaneous reaction of a patient to being addressed or having pain stimuli applied
    ↪ Helps mp the severity of impairments of consciousness (3-15 point scale)
  • Three domains:
    1. Eye opening
    2. Motor response
    3. Verbal response
  • For each you can get a rating and based on that they decide the severity of the injury
  • Low score = more severe, high score = less severe
  • Criticism: when it is administered differs - not ideal to predict longer term outcomes = might be incorrect
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12
Q

What is Post-Traumatic Amnesia? How do we split in two types?

A

Post-Traumatic Amnesia - loss of memory due to TBI
- The moment of accident forms a dividing line between the two parts of PTA
1. Retrograde Amnesia
2. Anterograde Amnesia

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13
Q

Retrograde amnesia

A

Amnesia about the time prior to the accident and the accident itself
- over time, RA ‘shrinks’ and the remaining amnesia concerns the period shortly before the accident
↪ result of interruption in the consolidation process

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14
Q

Anterograde amnesia

A

Occurs after the accident, as a result of which new info cannot be stored

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15
Q

What is PTA predictive of? How is PTA correlated with severity of TBI?

A
  • Duration of PTA often correlated with GCS but offers finer scalping
  • PTA more predictive of long-term cognitive status and neuroimaging findings (compared to GCS)
  • Most predictive of long-term cognitive status
  • Helps determine the presence and severity of a TBI
  • Increasing duration of PTA corresponds to more severe injury
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16
Q

What are some non-behavioural measures of TBI?

A
  • Neuroimaging and electrophysiological measures like EEG used for damage assessment
  • CT scans commonly used in acute stages for their cost-effectiveness and availability
  • MRI is preferable in subacute (stable phase) and chronic stages for its predictive power
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17
Q

What is neuropathology of TBI?

A
  • Effects develop over various timeframes, from mins to years
  • Very complex to find the biomarker (changes over time - graph) so difficult to predict outcomes
  • Nature of impairments depends on the timing of assessment
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18
Q

Penetrating head injuries

Causes of penetrating head injuries

A
  • Leading cause: gunshot wounds
  • But also, everyday objects like ball-point pens, chopsticks, door keys, etc
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19
Q

Penetrating head injuries

Mortality and severity

A
  • PHI mortality 6.6 times higher than Closed Head Injury
  • 36% dead on arrival or die in emergency unit
  • 41% of admissions for survivable injuries die within first 48 hours
  • 52% of survivors are severly affected
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20
Q

Penetrating head injuries

Types of injuries resulting in PHI

A
  1. Objects embedded in head (problematic: if you remove might cause imflammation which could result in epilepsy)
  2. '’Through-and-through’’ injuries: both entry and exit wounds
  3. Bone fragments often driven into the brain (tangential injury)
  • affect how they present problems but also their extent of recovery
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21
Q

Penetrating head injuries

What does neuropathology asses in case of PHI? Why is it important to have this info?

The second question ties to the next flashcard

A
  • Advanced imaging techniques show type and extent of PHI damage
  • Key issues: penetration location, trajectory, fragment scattering
    ↪ Affects the behavioural outcome
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22
Q

Penetrating head injuries

What factors affect the outcome PHI is going to have?

A
  • Physical qualities like speed, wobble, and malleability affect extent of damage
  • The speed and physical qualities of the object is most closely associated with the extent of tissue damage
  • High-velocity (>300 m/s) causes more extensive tissue damage (gunshot wounds)
    ↪ Immediate problems
  • Delayed effects like post-traumatic epilepsy and increased risk for cancer are associated with worse outcomes
    ↪ Long term problems
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23
Q

Penetrating head injuries

What could the tissue damage in PHI result in?

A
  • Extensive blood loss can lead to hypotension and hypovolemia, worsening primary damage
  • Local and general cerebral oedema and intracranial haematomas may develop
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24
Q

Penetrating head injuries

Neuropsychological effects

A
  • Deficits depend on lesion site and clinical history (previous problems?)
  • General impairments, including issues with attention and memory
  • Short-term memory is especially likely to be compromised, regardless of injury location
  • Larger lesions generally result in more widespread deficits
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25
Q

Penetrating head injury

How does PHI progress? What is permanent damaged and what improved with time?

A
  • Rapid gains observed in the first year or two post-injury
  • Further improvement is slow and mainly due to learned accommodations
  • Cognitive impairments like language disorders may improve but sensory defects (lower level…?) like visual blind spots presist
  • General effects of brain damage, such as distractibility, may improve but not return to pre-injury levels
26
Q

Closed head injuries

Definition, consequences, stages of damage

A
  • Non-penetrating injuries (falls, blunt head trauma etc.)
  • CHI typically results in more generalised brain injury
  • Damage occurs in stages: initial impact followed by secondary physiological processes
  • Long-term effects can take months to years to fully develop (mainly in mild TBI because they often don’t become apparent immediately)
27
Q

Closed head injuries

What are the factors that determine the extent of damage?

A
  • Severity of injury dictates the extent of damage
  • Biomechanics crucial in determining primary and secondary effects
28
Q

Closed head injury - primary effects

What is Diffuse axonal injury (shearing)? What is the cause?

A
  • White matter (axons) injuries diffused over the brain
  • Frontal or lateral impact often results in DAI
  • Often the result of rotating forces that cause axons to become torn or damaged (because of opposing forces)
    ↪ often combined with microhaemorrhages and axonal degeneration
29
Q

Closed head injuries - primary effects

What is affected if there is axonal damage (shearing) in the corpus callosum?

A
  • Damage to the corpus callosum - some axonal extension can be missing
    ↪ Damage extends far from focal site due to axonal disruption and inflammation
  • Leads to atrophy and corresponding neuropsychological dysfunction
  • Diminished speed of processing due to hemisphere integration issues
30
Q

Closed head injury - primary effects

Biomechanical features resulting from DAI

A
  • Shearing forces tear delicate vasculature
  • Hemosiderin, an iron-laden residue, shows in MRI for subacute and chronic injuries
  • Contusions (local bruising) or subdural haematoma concerning due to pressure on the brain surface
31
Q

Closed head injuries - primary effects

Coup and Contrecoup lesions

Another complication that can happen

A
  1. Various mechanical forces resulting from a blow to the head cause TBI
  2. A coup is damage at the site of impact
  3. Pressure resulting from a coup (where the injury happens) may push the brain to the opposite end or side of the skull, producing a contrecoup
    - Leads to injury in both sides
32
Q

Closed head injuries

What secondary injuries (effects) can be observed? What can be seen on brain scans?

A
  • Secondary Brain Injury: As damaging as initial injury due to physiological processes
  • Factors: Elevated intracranial pressure (ICP), brain swelling (edema - bleeding from some part of the brian), insufficient oxygen (hypoxia), insufficient blood supply (ischemia) - necrosis of brain tissue, fever (pyrexia), and infection
  • Brian scans look similar to Demensia patients who have also an increase of the volume of ventricles and the gyri and sulci increase as a sign of cell loss
33
Q

Closed head injuries

Cognitive and mental impact

A
  • Reduced mental speed, attention (related to slowing of info processing), cognitive efficiency
  • Impact on high-level reasoning and executive functions
  • Impaired memory (difficulty with remembering recent info, coming up with words, remembering appointments…)
  • Complaints of confusion, irritability, distractibility (attention) and fatigue
  • Social cognition changes: emotionally flat, not taking others into consideration, unable to adapt to social situations
34
Q

Closed head injuries

Sensory alterations

A
  • Impaired sense of smell (Anosmia)
  • Visual impairments: visual acuity reduced, field defects, double vision, prosopagnosia
  • Dizziness and balance problems
  • Hearing Defects: tinnitus, hyperacusis
  • Sensory hypersensitivity
35
Q

Types of CHI based on severity

A
  1. Mild TBI
  2. Moderate TBI
  3. Severe TBI
36
Q

Closed head injury

The most important association in mild TBI

A

Complex association between severity and outcome

37
Q

Is there a specific classification of mild TBI/concussion?

A
  • Controversy over definition and symptom duration
  • No universally agreed classification
  • Much more agreeablness on moderate and severe TBI’s classification
38
Q

Mild TBI

Criteria of the American Congress of Rehabilitation Medicine
(ACRM) for mild TBI?

A
  • Any period of loss of consciousness (LOC) lasting for 30 minutes or less
  • Any loss of memory for events immediately before or after the accident (Post-Traumatic Amnesia, PTA) not exceeding 24 hours
  • Any alteration in mental state at the time of the accident (e.g., feeling dazed, disoriented, confused)
  • Focal neurological deficits that may or may not be transient
39
Q

Mild TBI

Epidemiology

A
  • Over 1.5 million documented TBIs annually; ~80% are mild TBI (extremely common)
  • Stats based on hospital records, but an estimated 25% never visit the ER, likely making the real rate higher
  • Approximately half of the cases meeting research criteria for mTBI are never formally diagnosed
40
Q

Mild TBI

Neuropathology

A
  • Mechanical Forces and Cellular Changes: Mechanical forces that alter cellular physiology and anatomy, especially affecting the axons
  • Physiological Disruptions: Potentially permanent cellular function changes and acute inflammatory reactions, especially in white matter
41
Q

Mild TBI

How does mTBI progress and what can it result in?

A
  • Cognitive issues may not manifest until days or weeks aften an accident due to other injuries or medication
  • Most individuals recover within hours to weeks, particularly after sports concussions, but a small percentage have long-term issues
  • Even with cognitive improvement, symptoms like headaches, fatigue, and dizziness persist in many patients
  • Studies suggest that reaction time and neurophysiological measures may reveal subtle, long-term mTBI affects better
42
Q

Mild TBI

Why is it difficult to predict the outcomes? What can actually help to predict them?

A
  • Interactions between cognitive, emotional, and behavioural factors, that were present before the injury, make predictions challenging
  • Inconsistent findings on the role of Loss of Consciousness (LOC) in predicting cognitive outcomes
  • Post-Traumatic Amnesia (PTA), life events, and emotional distress can be predictive but lose strength over time
  • Age over 40, pre-existing conditions, and history of brain illness are red flags - the best predictors
  • Self-reported cognitive issues are more strongly related to emotional state and premorbid traits than actual cognitive
    impairments
43
Q

Mild TBI

Post-concussion syndrome

Definition, causes, cogniform disorder

A
  • Immediate symptoms and persistent symptoms lasting beyond 3 months, not consistent with formal assessments
  • Does not mean it’s malingering
  • Symptoms may be maintained or worsened by stress or depressive reactions at the time of the accident
  • Outcomes affected by a range of neurological, physical, and psychological factors (inadequate coping style, catastrophising)
  • Premorbid personality or psychiatric disorders can contribute to the chronicity of postconcussion symptoms
  • Cogniform disorder - patients with excessive cognitive complaints and/or unexpectedly poor cognitive performance given their severity of their injury (unconscious)
44
Q

Mild TBI

Whiplash syndrome

A
  • Common in car accidents
  • Typical symptoms include neck pain, occipital headache, back pain, and upper limb pain (but the symptoms are very varied)
  • Patients unlikely to meet criteria for concussion or mild TBI, most likely no actual brain injury in majority of cases
  • Mixed views on whether neck abnormalities can be objectively demonstrated
  • Discrepancies in evaluating the validity of complaints
  • Chronic pain is the most common persistent complaint (that’s mostly what distinguishes it from post-concussion syndrome)
  • Impact on sleep and cognitive function, mostly attention and memory, dizziness
45
Q

Mild TBI

Cognitive deficits in mild TBI

A
  • Early Stages Post Mild TBI: Moderate to severe communication, perceptual, or conceptual disturbances
  • Symptoms clear up for most but subtle defects may remain
  • Attention problems are most common, include poor concentration, distractibility, and mental fatigue
  • Sensory and perceptual issues often reported, including visual incoordination, photophobia (not able to deal with bright lights), dizziness, deafness, or tinnitus
46
Q

Mild TBI

Non-cognitive Impairments

A
  • Headaches are common, even in post-acute stage
  • Dysphoria and fatigue are very common
  • 35% prevalence of depression
47
Q

What is moderate TBI and what is its epidemiology?

A
  • Definitions vary in clinical criteria, including GCS scores (GCS score: 9-12 usually)
  • Few specific studies on moderate TBIs compared to mild or severe
  • 8-10% of all TBIs are moderate; some reviews suggest 7-28%
48
Q

Moderate TBI

Cognitive deficits

A
  • Ongoing cognitive deficits at six months, especially in information processing speed
  • Short-term memory deficits are common
  • Frontal and/or temporal bruising often results in behavioural changes (hyperorality, saying inappropriate jokes or vulgar comments…)
  • Temporal lobe damage may result in learning disorders or affective changes (lot of ups and downs but even completely flat mood)
49
Q

Moderate TBI

Progression and Outcome

A
  • Patients generally function independently
  • Many return to work but differ from their former selves
  • Reduced initiative in non-routine activities (related to frontal lobes deficit)
  • Emotional processing impaired, affecting relationships and motivation (lack the drive to engage, lack of insight in how affected they are especially 1 or 2 years after the injury)
50
Q

What is severe TBI and what is its epidemiology?

A
  • GCS score of 8 or less, loss of consciousness for 30 min or more, PTA for more than 24 h
  • Less than 10% of TBI victims are severely injured but present substantial societal costs
51
Q

Severe TBI

Cognitive deficits

A
  • Executive dysfunction: Impulsivity, lack of self-determination, lack of self-awareness
  • Memory deficits: Problems with long-term and short-term memory
  • Communication: Problems with word finding, reduced logical coherence and context awareness
52
Q

Severe TBI

Non-cognitive impairments

A
  • Depression and anxiety are very common in TBI patients, regardless of injury severity (more common later on when they gain more insight)
  • Tendency for these conditions to intensify over time
  • Often a reaction to physical and cognitive limitations
  • Higher rates of mania, paranoia, and schizophrenic-like symptoms
  • Increased personality disorders: borderline, avoidant, paranoid, OCD, narcissistic
53
Q

Severe TBI

Progression: Initial phase

A
  • Most patients show some progress but struggle with the severe impact of Traumatic Brain Injury (TBI)
  • Gradual improvement in physical status and cognition
  • Severe injuries lead to long-term pervasive deficits
  • Improvement in learning and other cognitive functions occurs but seldom reaches normal levels
54
Q

Severe TBI

Progression: >1 year

A
  • Improvement continues but at a slower pace, relying on new learning and compensatory strategies
  • Emotional and psychosocial aspects show minor improvements but largely remain static
55
Q

Severe TBI

Outcome

A
  • Reduced level of independence in daily activities and employment
  • Often persistent physical complaints e.g., headaches, dizziness, fatigue, pain
  • Return to previous employment levels is rare
  • Emotional and physical burdens placed on families
  • Social isolation and caregiver depression are common
56
Q

What other factors determine outcomes? - Moderators

A
  1. Age
  2. Repeated TBI
  3. Polytrauma
  4. Alcohol use
57
Q

How can age act as a moderator of the outcome of TBI?

A
  • TBI most frequent in under 35s, impacting social and employment outcomes
  • Early age TBI needs more intensive education and has poorer vocational outcomes
  • Increased odds of adverse outcomes, especially post-65
  • Aging brain characteristics contribute to worse outcomes, not just injury severity
  • Risk of cognitive decline (e.g. dementia) increases nearly 5 times for each 10 years of age
  • Increased rates of depression, psychotic disorders, and dementia in older patients
58
Q

Moderators

What is repeated TBI? What does it result in?

A
  • Second or more mild concussions have increasingly negative cognitive effects
  • A single TBI doubles the risk of future head injury
  • Chronic Traumatic Enceohalopathy (CTE)
59
Q

Chronic Traumatic Encephalopathy

A
  • Confirmed presence in athletes with repeated concussions
  • Subconcussive injuries can evolve into significant brain damage over time
60
Q

How can we demostrated CTE with boxing as an extreme example?

A
  • Even without KO history, boxers experience cognitive and motor symptoms
  • 20% of professional boxers develop CTE
  • MRI shows cerebral atrophy in boxers
  • High frequency of neuropathological abnormalities confirmed
61
Q

Moderators

Polytrauma

A
  • Head injuries often accompanied by trauma to other body parts
  • Impacts severity of neurobehavioral conditions
  • Cognitive deficits affect polytrauma outcomes
  • Multiple skeletal injuries hinder rehabilitation benefits for head-injured patients
62
Q

Moderators

Alcohol and Substance Use

A
  • TBI patients with prior alcohol abuse have poorer neuropsychological outcomes
  • Alcohol and polysubstance abuse are major contributors to the incidence of TBI
  • Fronto-temporo-limbic injury decreases impulse control and judgment, increasing likelihood of further substance abuse
  • Alcohol exacerbates severity of head injury, neuropathological changes, and outcomes, even accounting for other variables like vehicle crush and demographics

Clinical and Neuropsychology - 1 (21 decks)

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