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Neuro 1 > TBI > Flashcards

TBI Flashcards

1
Q

What is the most common cause of TBI in children?

A

falls and abuse

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2
Q

What is the most common cause of TBI in adolescents and young adults?

A

Falls, assault, and MVA

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3
Q

What is the most common cause of TBI in older adults?

A

FALLS

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4
Q

What is the difference between opened and closed injuries? Is one more serious than another?

A

open - penetrating type of wound (knife, gunshot, sharp object)
- skull fractured or displaced

closed - impact to head but skull is not fractured
- only cortical neuronal tissue is damaged

Open is worse b/c of infection risk plus debris

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5
Q

What happens to the meninges during open TBI? Closed TBI?

A

open - meninges are compromised and at risk for infection, bleeding, impaired CSF circulation

closed - meninges remain intact

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6
Q

What is meant by primary brain damage? What types of primary brain damage exist?

A

direct injury that results from mechanical issue at the time of trauma

focal and diffuse injury

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7
Q

Focal injury

A

localized to area under site of impact or site opposite of impact
- coup-contracoup injury

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8
Q

Diffuse injury

A

more widespread injury

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9
Q

hematoma

A

pool of clotted or partial clotted blood that congregates and settles in whatever space it is confined in
- due to rupture or damage to meningeal structures when in skull

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10
Q

Epidural hematomas

  • location
  • characteristics
  • intervention
A

location - between the dura mater and skull

characteristics - involve brief loss of consciousness followed by period of awareness and then crash
- unconsciousness (bad) - alert (better) - deteriorate (way worse)

intervention - craniotomies and hematoma evacuation

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11
Q

subdural hematomas

  • location
  • characteristics
  • intervention
A

location - rupture to the cortical bridging veins between dura and arachnoid

characteristics - blood slowly leaks over several hours or weeks and symptoms similar to CVA

intervention - small clots reabsorbed and larger ones require surgical removal

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12
Q

Which type of focal injury is seen in elderly after falls w/ blow to the head?

A

subdural hematomas

- they think they are fine and family member will start to notice something is off and then go to ER to find bleed

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13
Q

subarachnoid hemorrhage

  • location
  • sequela
A

location - between arachnoid and brain tissue

sequela - vasospasm

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14
Q

intracerebral hemorrhage

  • location and cause
  • sequela
A

location and cause - within the brain itself from significant brain injury

sequela - seizures, stroke-like presentation

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15
Q

What type of hemorrhage is the most life-threatening?

A

subarachnoid hemorrhage

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16
Q

What is a brain contusion? How does it present?

A

bruising on the surface of the brain is sustained at time of impact

presents on side of impact or opposite side of impact

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17
Q

coup lesion

A

contusion on the same side of the brian as the impact

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18
Q

contrecoup lesion

A

surface hemorrhages on the opposite side of the brain trauma as a result of deceleration
- whiplash of the brain

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19
Q

Which is typically worse in damage, coup or contrecoup injuries? Why?

A

contrecoup injuries are worse because of momentum of brian towards the impact side is little than picks up speed (there is more room) and slams into opposite sides
- PHYSICS!

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20
Q

What areas are most commonly involved in coup contrecoup injuries?

A

anterior poles and underside of temporal and frontal lobes

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21
Q

What is a diffuse axonal injury (DAI)? What typically causes it?

A

widespread shearing and retraction of damaged axons that results in traumatic “micro bleeds”
- significant neurological involvement and poor prognosis

caused from HUGE acceleration, deceleration, and rotational forces (MVA most common)

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22
Q

What areas are most suspectable to damage from a DAI?

A

corpus callosum
basal ganglia
brainstem
cerebellum

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23
Q

What occurs with secondary brain damage?

A

global reduction of O2 in the body so brain starts to die

- can further lead to reduction in CO and/or ischemic event

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24
Q

What occurs with secondary brain damage caused from a TBI?

A

electrolyte imbalance and mass release of damaging neurotransmitters
- causes apoptosis

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25
Q

What occurs with secondary brain damage not caused from a TBI?

A

hypoxic/ischemic injury

swelling/edema - increased ICP

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26
Q

anoxic vs hypoxic brain injury

A

anoxic - no O2 to brain

hypoxic - little O2 to brain

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27
Q

What causes anoxic/hypoxic brain injuries?

A

Lack of O2 blood to brain

  • cardiac arrest, CO2 toxicity, near drowning, internal bleeding
  • anything that causes systemic hypotension
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28
Q

What are anoxic/hypoxic brain injuries associated with?

A

poor prognosis for cognitive function

- lower expected functional outcomes

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29
Q

What areas of the CNS are more vulnerable to oxygen depletion?

A

hippocampus
cerebellum
basal ganglia

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30
Q

tertiary blast injury

A

blast causes you to fall and hit head like TBI

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31
Q

secondary blast injury

A

result of shrapnel

  • cause multifocal injuries because of multiple shrapnel pieces
  • HIGHER risk of infection
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32
Q

primary blast injury

A

direct effect of blast overpressure on organs

- blast causes brain to move

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33
Q

What type of brain damage usually occurs with primary blast injuries?

A

diffuse brain damage

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34
Q

What happens to CSF or venous pressure after primary blast injury?

A

increase

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35
Q

What type of diagnostic imaging is usually included in TBI workup?

A
  • MRI
  • CT - better than MRI
  • PET - shows brain function
  • EEG - used if concerns for seizures
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36
Q

What are the major goals of medication management for acute TBIs?

A
  • decrease BP and ICP
  • decrease intracranial bleeding
  • anti-seizure
  • decrease body temp
  • decrease infection rate
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37
Q

When is ICP elevation a risk post TBI?

A

highest risk during acute phase but can occur several months later

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38
Q

Why is an increase in ICP problematic?

A
  • compress brain tissue
  • decrease perfusion to brain tissue
  • possible herniation
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39
Q

What is normal ICP and what is abnormal ICP?

A

normal - 5-10 mmHG

abnormal - > or = 20 mmHg
- use caution when > or = 15 mmHg

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40
Q

T/F - you cannot treat a patient with ICP 20 mmHg or above

A

true

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41
Q

What activities have the potential to increase ICP?

A
  • full supine or Trendelenburg
  • cervical flexion
  • percussion and vibration
  • Valsalva (coughing, sneezing, holding breath)
  • exertional activities
  • quick elevating head of bead
  • supine to sit
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42
Q

What are the signs and symptoms of elevated ICP?

A
  • decreased responsiveness, irritability
  • impaired consciousness
  • severe HA, seizures - impaired sensory and motor function
  • vomiting
  • papilledema, pupillary changes, impaired eye movement
  • change in vitals - increased BP, decreased HR, irregular RR
  • posturing - decerebrate, decorticate, flaccid
  • changes in speech
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43
Q

What are the signs and symptoms of elevated ICP in infants?

A
  • bulging fontanels
  • increased head circumference
  • high pitched cry
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44
Q

How is elevated ICP managed?

A

medication and ventricular peritoneal shunting if needed for permanent correction

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45
Q

What is abnormal ICP?

A

> or = to 20 mmHg

- Do not treat patients w/ elevated ICP 20 mmHg or above

46
Q

Increased pressure can _______ brain tissue, _________ perfusion to brain tissues or possible herniation

A

compress, decrease

47
Q

How are TBIs and seizures related?

A

increased risk of seizure after TBI

48
Q

What are some examples of events that could trigger a seizure post-TBI?

A
  • stress
  • poor nutrition
  • electrolyte imbalances
  • missed medications or drug use
  • flickering lights
  • infection
  • fever
  • anxiety
49
Q

common S & S of seizures

A
  • focal or diffuse twitching, jerking; stiffening
    • or - loss of consciousness
  • absent staring
50
Q

Can you treat a patient who is on medication to lower body temperature after a TBI?

A

No - they are too medically unstable

51
Q

How are seizures managed post-TBI?

A

medications and continuous electroencephalogram (cEEG)

52
Q

When is it safe to mobilize a patient after a seizure?

A

more than 24 hours after being seizure-free

53
Q

What is PAID? What are characteristics?

A

Paroxysmal Autonomic Instability and Dystonia

- sympathetic (fight or flight) system goes into overdrive

54
Q

What type of TBI is PAID seen with?

A
  • severe TBI

- glascow coma score 3-8

55
Q

clinical S & S of PAID

A
  • tachypnea
  • tachycardia
  • HTN
  • Diaphoresis
  • Decorticate/Decerebrate Posturing
  • agitation
56
Q

How is PAID diagnosed? How is it managed?

A

diagnosed through clinical obeservation

managed w/ medication that suppresses sympathetic nervous system

57
Q

What do you do if a patient is suffering from PAID?

A

No treatment if patient is having active issues (storming)

58
Q

Describe the relationship between heterotopic ossificans (HO) and TBI. What increases risk?

A

10-20% of TBI and increased risk if TBI polytrauma results in fracture near joint line
- common in large joints

59
Q

When does heterotopic ossification occur after TBI?

A

~ 4-12 weeks after brain injury

60
Q

What is Heterotopic Ossification clinical presentation?

A
  • loss of ROM w/ hard end feel and pain
  • local erythema, pain w/ movement, swelling, warm to touch (like DVT)
  • severe HO may result in vascular and/or nerve compression
61
Q

What is difference between HO and DVT when it comes to ROM?

A

DVT ROM will not have hard end feel

62
Q

How is HO managed?

A
  • maintain ROM and prevent further complications
  • medications
  • surgical excision after it has stopped growing
63
Q

What is didronel used for?

A

prevents calcium from being deposited in bony matrix to prevent HO

64
Q

What is used for symptom management for HO?

A

anti-inflammatories

65
Q

What is the most common and debilitating cognitive deficit following TBI?

A

attention deficits

65
Q

What are the 5 categories of attention?

A
  • focused
  • sustained
  • selective
  • alternating
  • divided
65
Q

S & S of impaired attention

A
  • unable to engage on relevant info
  • unable to sustain attention to task
  • unable to switch to new task
  • unable to resist distraction
  • unable to multitask
  • unable to manipulate mental info while maintaining overarching goal in mind
66
Q

What dysfunction is most common when there is damage to prefrontal cortex?

A

executive function deficits

67
Q

general characteristics of executive function deficits seen post-TBI

A

impairment to:

  • volition/planning
  • problem solving
  • insight (impulsive)
  • social pragmatics
  • self-regulation
68
Q

general characteristics of memory deficits seen post-TBI

A
  • retrograde (unable to recall) and/or anterograde (unable to create new memories) amnesia
  • posttraumatic amnesia
  • short term > long-term
  • Declarative (dates, time, history) and procedural (skills) memory often impaired
69
Q

T/F- TBI patients have more issues with long term memory over short term memory.

A

false - short term > long term memory

70
Q

If TBI patient is having issue with speech, it is more likely due to _______ impairment instead of ______

A

cognitive impairment instead of aphasia

71
Q

general characteristics of language deficits seen post-TBI

A
  • non-aphasic and more cognitive impairment
  • disorganized and tangential oral and written communication
  • imprecise language
  • word-retrieval difficulties
  • disinhibited language
72
Q

What is the most enduring and socially disabling of impairments after TBI?

A

behavioral issues

- usually temporary and can be managed

73
Q

What types of behavioral issues can be seen post-TBI?

A
  • sexual disinhibition
  • apathy
  • aggressive disinhibition
  • agitation
  • hyperactive, restless
  • low frustration tolerance
  • depression
  • EASILY OVER-STIMULATED
74
Q

What are the 2 common syndromes after frontal lobe damage from TBI?

A

orbitofrontal lobe syndrome - disinhibited
- lack of restraint manifested in disregard of social conventions, impulsivity, and poor risk assessment

frontal convexity syndrome - apathetic
- showing or feeling no interest, enthusiasm, or concern

75
Q

Signs of orbitofrontal lobe syndrome

A
  • impulsive behavior
  • inappropriate jocular affect, euphoria
  • emotional liability
  • poor judgement and insight
  • distractibility
76
Q

Signs of Frontal Convexity Syndrome

A
  • apathy (lack of interest, enthusiasm, concern)
  • indifference
  • motor preservation and impersistence
  • stimulus-bound behavior
  • motor programming deficits
  • poor word list generation
77
Q

Diffuse injuries more so characterized by ________ and ________ deficits over true strength deficits

A

motor control and coordination

78
Q

What types of tone abnormalities can be seen post-TBI

A
  • flaccidity, rigidity, or hypertonicity
  • decorticate and decerebrate rigidity
  • primitive and tonic reflexes
79
Q

Decorticate Rigidity

A

LE extension and UE flexion

80
Q

Decerebrate Rigidity

A

LE and UE extension

81
Q

What sensory deficits are most common post-TBI?

A

proprioceptive and kinesthetic deficits

82
Q

What cranial nerves are commonly found to be damaged post-TBI?

A
  • CN 1 - olfactory
  • CN 2 (optic), 3 (oculomotor), 4 (trochlear), 6 (abducens)
  • CN 5 - trigeminal
  • CN 7 - facial
83
Q

What CN is commonly affected by concussion?

A

CN 1 olfactory

84
Q

conjugate gaze palsy is injury to what?

A

CNS

85
Q

unilateral gaze palsy is injury to what?

A

PNS

86
Q

tonic (constant) downward gaze is injury to what?

A

severe injury to thalamus, midbrain or pons

87
Q

tonic (constant) upward gaze is injury to what?

A

severe injury to both hemispheres

88
Q

What is an indication of seizure activity when it comes to the eyes?

A

rapid horizontal eye movement

89
Q

What is the common culprit of PNS gaze abnormalities? How will the patient present?

A

abducens nerve - patient will have unilateral gaze towards adduction

90
Q

What structure is damaged if the patient has monocular blindness and absent pupillary response?

A

optic nerve

91
Q

Why is oculomotor and trochlear nerve damage less common?

A

damage occurs to the muscle bellies and tendons vs the nerve

92
Q

What CN are commonly damaged due to their superficial proximity?

A

trigeminal and facial nerve

93
Q

Where is trigeminal nerve damage common and what are the presentations?

A
  • Peripheral injury to where divisions leave orbit common

- Results in loss of sensation to the nose, eyebrow and forehead

94
Q

Where is facial nerve damage common and what are the presentations?

A
  • Peripheral injury when temporal bone damaged

- Muscle weakness, loss of tear production, decreased saliva secretion, and taste

95
Q

Vestibular rehabilitation may take up to ______ as long than those without TBI compared to other vestibular patients

A

3x

96
Q

Where is the damage if a patient is unable to perform sensory integration for balance?

A

brainstem or cortex involving vestibular pathways

97
Q

common ANS symptoms seen with TBI

A
  • HR variability
  • RR variability
  • BP changes
  • elevated body temp.
  • excessive sweating, salivation, tearing
  • dilated pupils
  • vomiting
  • anxiety, panic disorder, PTSD
98
Q

What predicative capabilities does the GCS have as it relates to TBI mortality?

A

lower the score the higher the mortality rate

- GCS of 3 at initial presentation results in 65-100% TBI mortality rate

99
Q

T/F - A mild TBI is a concussion

A

true

100
Q

Mild TBI: GCS, LOC, alteration of consciousness, post-traumatic amnesia, imaging

A
  • GCS - 13-15
  • LOC - 0-30 minutes
  • brief (<24 hours) alteration of consciousness
  • post-traumatic amnesia < 1 day
  • normal imaging
101
Q

Moderate TBI: GCS, LOC, alteration of consciousness, post-traumatic amnesia, imaging

A
  • GCS - 9-12
  • LOC - > 30 min but < 24 hours
  • alteration of consciousness > 24 hours
  • post traumatic amnesia > 1 day but < 7 days
  • normal or abnormal imaging
102
Q

Severe TBI: GCS, LOC, alteration of consciousness, post-traumatic amnesia, imaging

A
  • GCS - 3-8
  • LOC - > 24 hours
  • alteration of consciousness > 24 hours
  • post-traumatic amnesia > 7 days
  • normal or abnormal imaging
103
Q

What does Disability Rating Scale measure?

A

impairment, function, and participation

Looks at 4 major categories

  • consciousness
  • cognitive ability
  • independence
  • employability
104
Q

What is scoring for Disability Rating Scale and what can it predict?

A

30 point scale and higher scores represent high level of disability

  • can predict return to work potentional
105
Q

What is the Glasgow Outcome Scale mainly used for?

A

used more for research vs clinical

- classifies global outcomes for TBI patients

106
Q

How can patients generally be described when falling under severe, moderate, and good recovery categories for Glascow Outcome Scale?

A

Severe - dependent

Moderate - independent but participation in community is limited

Good - can return to work, school, etc but may need some accommodations

107
Q

Negative prognostic indicators for TBI (10)

A
  • Older age
  • Female (worst recovery compared to men)
  • GCS score
  • Length of PTA
  • Acquired injury (vs Traumatic)
  • Lower education level/pre-injury IQ
  • Delayed or inability to use neurostimulants
  • Presence of pre-injury psychological issues or substance abuse
  • GOS: Level 1-3
  • Initial GCS: 3-8
108
Q

Severe TBI negative prognostic factors (5)

A
  • older age
  • absence of light reflex
  • presence of extensive subarachnoid hemorrhage
  • sustained elevated ICP
    • midline shift

Neuro 1 (11 decks)

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