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Neuropsych Board Prep > Traumatic Brain Injury > Flashcards

Traumatic Brain Injury Flashcards

1
Q

What causes moderate to severe traumatic brain injury?

A

Damage to brain tissue causes by external mechanical force, as evidenced by LOC, PTA, positive neuroimaging, or objective neurologic finding

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2
Q

What is a mild TBI (mTBI/concussion)?

A

Traumatically induced physiological disruption of brain function that results in a graded set of clinical symptoms that most often resolve spontaneously

Alteration or LOC and other transient neurologic signs can occur

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3
Q

Describe primary pathological effects associated with a TBI injury?

A
  • Occurs immediately
  • Results from linear and/or rotational forces
  • E.g., skull fracture, contusion, subarachnoid hemorrhage, mechanical injury to axons and blood vessels
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4
Q

Where is the skull are focal injuries most common?

A

Frontal and temporal lobes

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5
Q

Where is diffuse axonal injury most common?

A

Gray-white matter junction/

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6
Q

What are secondary injuries that occur directly or indirectly from a TBI?

A

Hypoxia, ischemia, swelling/edema, hypotension, mass lesions, raised intracranial pressure, and poor cerebral perfusion pressure

Can be gradual or accelerate quickly

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7
Q

At what ages is TBI most common and what are the most common causes?

A

0-4 years: child abuse
15-19 years: MVA
65 and older: falls

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8
Q

What are additional TBI risk factors besides age?

A

Alcohol/substance abuse, high-risk behavior, male gender, history of prior TBI, psychiatric illness, ADHD, lower SES/education

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9
Q

Is brain injury usually the cause for symptom persistence beyond 3 months after mild TBI?

A

No, typically the cause is multifactorial and not due to brain injury as symptoms typically resolve by this time

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10
Q

What are risk factors that increase the risk of persistent problems after mild TBI?

A
  • Prior hx of neurologic injury
  • Hx of recent or multiple mild TBIs
  • Hx of chronic medical condition
  • Polytraumr/chronic pain
  • Misattribution bias
  • Potential for secondary gain
  • Hx of psychopathology
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11
Q

How many people sustain a TBI each year?

A

1.7 million

52,000 die, 275,000 are hospitalized, and 1.365 mil are treated and released from ED

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12
Q

How many injuries are mild TBI compared to moderate/severe TBI?

A

80% of injuries are mild TBI

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13
Q

Why do a small number of patients who present with mild TBI later regress?

A

Due to epidural or subdural hematoma.

Those over age 60 are 4 times more likely to develop a chronic subdural hematoma d/t widening of cortical sulci with aging and increased vein vulnerability

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14
Q

What are those patients with mild TBI who have positive neuroimaging referred to as?

A

Complicated mild TBI

Functional outcome is similar to moderate TBI

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15
Q

What is the diagnosis of TBI based on?

A

Parameters in the medical/historical records- not neuropsych findings

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16
Q

What tools can be used to classify TBI?

A
  • Glascow Coma Scale
  • Length of post-traumatic amnesia
  • Time to follow commands
  • Radiological findings
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17
Q

What is the imaging method of choice in acute care?

A

CT bc it is widely available and sufficient for identifiying findings that require urgent intervention

MRI in the subacute period (>3 months) is reliable for determining amount of persistent encephalopathy

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18
Q

Are focal neurologic signs used for ratings of severity?

A

No because they may or may not be transient

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19
Q

What are non-TBI factors that can influence common markers of severity in the acute stage?

A

Developmental immaturity, intoxication, internal/peripheral injuries, medications, metabolic disturbances, substance withdrawal, and infection

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20
Q

What are common complications following TBI?

A

Cranial nerve injury, sensory changes, fractures/internal injuries

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21
Q

How long do individuals with mod to severe TBI experience PTA for?

A

days, weeks, or even months post-injury

Exception: with penetrating TBI, some patients sustain severe injuries but may not lose consciousness nor experience persistent PTA

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22
Q

What are treatment goals in the acute period of a TBI?

A

Medical stabilization, emergent surgical intervention, minimization of secondary injury

23
Q

What are some treatment recommendations?

A

Maintain a low-stimulation environment

Avoid the regular use of neuroleptic meds and certain anticonvulsants

24
Q

When is it appropriate to perform a brief neuropsy exam to establish a post-injury baseline?

A

When the patient has a measureable level of continuous memory for 2-3 consecutive days

25
Q

What is the long-term recovery like for those with moderate to severe TBI?

A

it is variable. More severe injuries have a higher probability of long-term impairment. Many patients with mod-severe TBI have good functional recovery and can return to independent living.

26
Q

What are some important issues a neuropsych exam should address in this population/

A

Need for supervision, guardianship, conservatorship, and attentdant care

Restrictions or acommodations regarding school, work, driving, etc.

Appropriateness of current treatment and need for additional services

27
Q

How long does recovery take after mod to severe TBI?

A

May take more than 12 months but majority of recovery happens in the initial months postinjury

Over time- social support and access to resources has more influence on recovery than injury seerity

28
Q

What are two approaches to cog rehab?

A

Restorative and compensatory skills training

29
Q

What are typical neuropsych results in mod to severe TBI?

A
  • Intelligence/achievement: unlikely to be affected but injury in infancy/childhood may result in IQ and academic consequences
  • Attention/concentration: after resolution of PTA, decreased ability to multitask and sustain/divide attention
  • Processing speed: Most commonly affected cognitive ability d/t impact on WM pathways
  • Language: Persistent aphasia is uncommon unless a focal injury but language pragmatics may be affected as well as naming and phonological processing
  • Visuospatial: Affected w/focal injuries
  • Memory: Reduced declarative mem w/ encoding and retrieval
  • Executive functions: problems with organization, planning, mental flexibility, and judgment are common
  • Sensorimotor: Reduced psychomotor speed and coordination
  • Emotion: Depression and anxiety are common
30
Q

What is the Kennard principle?

A

Suggests that younger brains have more “plasticity” and therefore a better prognosis following injury.

Researches have FAILED to confirm this in the context of diffuse brain injuries

31
Q

What are delayed consequences of TBI in a young child?

A

Full impact of injury may not be apparent until the patient reaches a developmental stage that requires more demands on cognition

32
Q

Why is family and social support important?

A

Access to resources and strong social support leads to better functional outcomes in children.

33
Q

Why are elderly patients with a TBI more prone to SDH?

A

Due to anticoagulant or antiplatelet medication

34
Q

What is the outcome of older patients who sustain a TBI?

A

Require prolonged supervision, attendant care, and/or placement in an extended care facility

Those with a mod/severe TBI at a younger age are at an increased risk for developing dementia later in life

35
Q

What are acceleration/deceleration injuries?

A

Occur following unrestricted movement of the head creating tensile, shear, and compressive strains that often follow high-speed events

36
Q

What is the brain reserve hypothesis?

A

There is variability across individuals with regard to resilience and susceptibility to brain injury/poor outcome.

Those who have a hx of prior neurologic injury/illness are at a higher risk for complicated outcome following TBI

37
Q

What is the cognitive reserve hypothesis?

A

Emphasizes the potentially protective effects of higher premorbid intelligence and better quality of education prior to injury

38
Q

What is cerebral prefusion pressure?

A

A measure of the amount of blood flow in the brain.

Mean systemic arterial blood pressure- ICP

Level and duration of reduced CPP is a main determinant in the severity of cerebral damage

39
Q

Is the presence/absence of loss of consciousness a predictor of outcome?

A

No, it has actually been de-emphasized in recent years because of its inconsistent relationship with outcome

40
Q

What is a diffuse axonal injury?

A

Caused by the stretching of myelinated axons between brain tissues of differing densities

It is strongly related to the effects of secondary injury

it evolves over time

Diffusion tensor and weighted susceptibility imaging shows some promise in evaluating DAI

It is a neuropathological diagnosis determined via microscopic analysis on autopsy

41
Q

What is the dose-response fallacy?

A

False assumption based on the concept of the magnitude of a stressor and subsequent response of the receptor, which leads to the false conclusion that mild TBI results in permanent milt to moderate cog impairments because mod to severe TBI results in persistent mod to severe impairments

42
Q

What is an epidural hematoma?

A

Cause by rupture of arteries between the skill and dura. Can result in a rapidly expanding hematoma that causes the compression of brain tissue.

Can lead to tnetorial herniation and death. Some patients recover similar to mild TBI if it is evacuated quickly, but if it is not than there is a high morbidity and mortality.

43
Q

What is the Glascow Coma Scale?

A

Assesses the responsiveness in patients who have sustained brain injury/

Three paramteres: eye opening, motor repsonse, and verbal response.

Scale ranges from 3-15.

Scores <8= severe injury
Scores>13= mild injuries

44
Q

What term is used with a GSC >13 but positive neuroimaging?

A

Complicated mild TBI

45
Q

Ia GSC a good predictor of long term outcome following TBI?

A

No because it can be affected by non-brain injury related factors too

46
Q

How is ICP measured?

A

By recording subarachnoid fluid pressure.

47
Q

What is a neurometabolic cascade?

A

Following TBI, a process of iconic shifts, impaired neuronal function and connectivity, and altered brain metabolism, disruption of normal brain function/signal transmission, and indiscriminate NT release can occur.

48
Q

What is a nonpenetrating vs. penetrating TBI?

A

Closed head injury vs. open head injury.

Nonpenetrating: dura and skull remain intact.
Penetrating: Breach of dura mater

49
Q

What is postconcussion syndrome?

A

WHO discourages the use of this term because it does not meet criteria for a syndrome

Symptoms ascribed to PSC are nonspecific and overlap with other variable symptom constellations

50
Q

What is posttraumatic amnesia?

A

Original definition: amount of time following injury that an individual remains confused and exhibits anterograde amnesia (including coma)

Newer definition: Include the period of confusion following the TBI but does not count a coma or unconsciousness

Length of PTA is considered to be the most robust predictor of outcome in TBI!!!

51
Q

How common are posttraumatic seizures?

A

For nonpenetrating TBI they were ucnommon (5%)

Seizures the first week following nonpenetrating TBI are not predictive of long-term risk for epilepsy

Penetrating brain injury is a sig risk for seizure (30-50%)

52
Q

What causes a subarachnoid hemorrhage?

A

Mulitple causes: brain injury, cerebral aneurysm, AVM, and HTN

Associated with poorer outcome in mod to severe TBI

53
Q

What is a subdural hematoma?

A

Caused by rupture of bridging veins between sulci on the upper surface of the brain

Commonly found in frontal and anterior temporal lobes in high speed injuries

54
Q

What does “time to follow commands” mean?

A

Amount of time following a TBI in which the pt is unable to follow simple motor commands.

Assessment is challenging because it must take into account sedation and paralysis

Emergence from a minimally responsive state corresponds to a 6 on the motor subscale of the GSC

Neuropsych Board Prep (32 decks)

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