Week 7 - Intro to TBIs Flashcards

1
Q

Traumatic brain injury definition

A

“when a sudden, external, physical assault damages the brain”

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2
Q

TBI rates

A

In USA – 1.4 million ind. are treated for TBI in EDs each year
* 27,000 are hospitalized
* 52,000 die from their injury

Most common causes:
* In Adolescence and YA – Motor Vehicle Collisions
* In older ages – Falls

More common in men than women

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3
Q

2 primary types of TBI

A

Closed BI: non penetrating injury to the brain with no break in the skull.

Penetrating BI: penetrating or open head injuries where there is a break in the skull

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4
Q

Closed BI: injury results from

A

Rapid forward and backward movement of brain in skull = tearing and
bruising of brain tissue and blood vessels

Coup contrecoup – (common in car accidents)
* Coup = point of impact
* Contrecoup = injury of opposite side

Diffuse Axonal Injury - (axons have been stripped, sheared, etc.)
e.g., car crash, falls, sports, shaken baby syndrome

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5
Q

Penetrating BI: injury results from

A

Penetrating objects, & skull bone fragments damaging brain tissue and
blood vessels = deprivation of normal blood supple (ischemia),
accumulation of blood (hemorrhage)

  • Cognitive impairments tend to be more focal
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6
Q

Diffuse Axonal Injury (DAI): definition and causes

A

“the shearing (tearing) of the brain’s long connecting nerve fibers (axons) that happens when the brain is injured as it shifts and rotates inside the bony skull.”

CAUSES:
* Damage to white matter
* Changes are microscopic
* Can lead to disorders of consciousness
(persistent vegetative state, coma)
* Difficult to see on CT Scan or MRI
* Can occur without other visible damage

3 grades

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7
Q

Time as mechanisms of injury

A

primary injury –> secondary injury

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8
Q

Chronic Traumatic Encephalopathy (CTE)

A

Produces neurodegeneration due to repeated head trauma

Prevalence in athletes who participate in contact sports and experience frequent and repeated head trauma (esp with young kids without fully formed skulls)

Can be confirmed by postmortem examination of tissue. Would see:
* abrnormal tau protein accumulation
* reduced brain volume
* ventricular enlargement (things are getting stuck, body not cleaning as it should, not as protective)

Mood and cognitive impairment can appear years after the injuries occured
* Characteristic deficits include - dysexecutive functioning (no impulse control) and mood lability

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9
Q

Recovery process

A

Ask about last memory before accident, and first memory after accident. trying to understand thier PTA episode

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10
Q

Classification system for TBI

A

Look at:
* duration of unconciousness
* glasglow coma scale
* Post traumatic amnesia

Classify as mild, moderate, severe

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11
Q

Glasgow coma scale

A

Look at eye opening, motor response, and verbal response

Limitations:
* Substance use
* Administered drugs
* Intubation
* Injury to eye
* Hemiplegia
* Language

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12
Q

Post-traumatic amnesia

A

State of confusion and disorientation that occurs immediately after TBI, is a part of the healing process –> brain focused on surviving (breathing) not memory

Brain is unable to form continuous day to day memories – Memory is the slowest part of conscious mind to recover

Behaviorally:
* Confused and disoriented (may recall their name or semantic knowledge)
* Agitation & aggression
* Inability to recognize loved ones
* Childlike/clingy behavior (almost like imprinting)
* Confabulation

NOTE:
* Can be very difficult for family members = provide education and reassurance
* Goal is to support re-orientation and sense of safety
* Do NOT ask them to recall the injury – they cannot do this!

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13
Q

Rancho Los Amigos Scale – Revised (RLAS-R)

A

When they are confused/agitated –> likely to be coming out of PTA

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14
Q

Cognitive recovery by TBI Severity

A

Most growth is within 6-12 months, after 2 years just focus on coping with injury

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15
Q

Dose-Response Relationship

A

Most well-designed studies, using a representative, non-clinically referred study sample show…

  • Cognitive changes after mild TBI resolve within weeks to about 3
    months at most spontaneously without treatment
  • changes tend to persist ≥ 2 years following moderate to severe TBI.
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16
Q

Non-injury risk factors that influence TBI outcomes

A
  • Pre-injury Psychiatric status & Conduct issues/incarceration –> Negatively effect outcome, can prolong symptoms.
    –> if anxious/depressed before, will likely be overly aware of symptoms after
  • Age at Injury
  • Level of Education (more education means larger cognitive reserve, can loose more cognition and still be smart)
  • Stable employment 6 months pre-injury –> Best predictor of return to employment post-injury
  • Marital status – thought to be a proxy for perceived social support
  • Other non-neurological injuries sustained – physical injuries can prevent return to meaningful activities
17
Q

Post-Concussion Syndrome vs. Somatization

A

Conscious attempt:
* primary gain (factitious disorder)
* secondary gain (malingering)

Unconscious attempt:
* somatic symptoms and related disorders

18
Q

MMPI-2-RF and Post-Concussion Syndrome vs. Somatization

A

FBS: Symptom Validity Scale — Noncredible somatic and cognitive complaints

RBS: Response Bias Scale — Exaggerated memory complaints