39. Neuropsych Sequelae of TBI Flashcards

1
Q

mechanisms of injury that occur as a result of TBI?

A
  • contusions
  • diffuse axonal injury (inertial)
  • impact forces (coup/contre-coup)
  • secondary injuries
  • neurochemical vulnerability (dysreg of nT systems)
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2
Q

when in the course of the TBI do secondary injuries appear?

A

later in the course.

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3
Q

distribution of TBI by age group?

A

peak in late teens/20s/30s (driving) and again in old age (falls)

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4
Q

definition of TBI. what does it result in?

A

def: force acting on the brain
result: disturbance in level of consciousness
(LOC not required)

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5
Q

good news and bad news about TBI?

A

GOOD: decr rate of mortality from TBI over past 30 yrs (we are saving more people)
BAD: incr number of young, otherwise healthy ppl with chronic neuropsych disabilities

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6
Q

is there a direct correlation between severity of TBI and clinical course?

A

generally there is a correlation, but sometimes people do much better/worse than severity of injury would predict.

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7
Q

what 3 datapoints do we use to categorize severity of TBI?

A
  • duration of LOC
  • Glasgow score
  • duration of post-injury amnesia
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8
Q

difference between Mild TBI and Complicated Mild TBI?

A

Complicated Mild has + findings on imaging

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9
Q

relationship between neuropsych syndromes and TBI

A

TBI greatly increases risk of dev neuropsych syndromes (approx 50% will dev a neuropsych disorder)

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10
Q

how do contusions affect neural pathways?

A

can cause damage to white matter tracts: not as well preserved after TBI. seen on a scan compared to healthy control.

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11
Q

someone is anticoag and hits their head: recommendation?

A

definitely should be evaluated: even small bumps to someone who is anticoagulated can cause cranial hemorrhage

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12
Q

DAI (though diffuse) primarily affects what parts of hte brain?

A

sub-cortical white matter, corpus callosum

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13
Q

DAI: evolution?

A

damage at time of injury and evolves over time: have scans from 1d, 1w, and 4y post-injury and there is progressive loss of projections from corpus callosum to cortical areas.

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14
Q

what is the difference between a primary and a secondary injury?

A

Primary: occurs immediately (contusions, hemorrhage, DAI)
Secondary: evolves over time (release of nTs, edema, ischemia, hypoxia, incr ICP)

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15
Q

3 major categories of neuro psych sequelae as a result of TBI?

A
  • dys-executive problems (social comportment, less motivation, decline in exec cognitive function like memory, attention, information processing)
  • other cog deficits
  • psychiatric disorders
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16
Q

what is the most common cognitive complaint after TBI?

A

memory. most commonly working memory, short term memory, encoding

17
Q

in addition to memory and loss of exec function, what other problem is seen post-TBI?

A

dementia

18
Q

what does this post-TBI dementia resemble?

A

alzheimer’s. neuronal loss, gliosis, tau deposition

19
Q

what predicts the neuro (psych/cognitive) sequelae?

A

the profile of the injury, the area damaged

20
Q

lateral orbitofrontal circuit: controls what?

A

social comportment.

impulsivity, irritability, affect, awareness

21
Q

anterior cingulate and medial frontal circuits control what?

A

motivation. (interest, initiative, drive)

22
Q

dorsolateral prefrontal circuit controls what?

A

Exec functions: planning, problem solving, working memory